摘要
目的研究血管内皮细胞(VEC)增殖过程中碘离子(I-)与丝裂原活化蛋白激酶1(MEK1)表达及其磷酸化的关系,探讨高碘促VEC增殖效应的作用通路。方法 1将体外培养的VEC分为空白对照组和不同碘离子浓度的实验组。2采用蛋白质印迹技术(Western blot)检测不同碘离子浓度培养环境中MEK1蛋白表达量及磷酸化水平。结果 1在300μg/L碘离子浓度组,MEK1蛋白相对表达量高于其他组(P<0.05)。2 500μg/L、1 000μg/L碘离子浓度可促进MEK1(Ser298位点)磷酸化水平上调(P<0.05)。3各实验组MEK1(Thr286位点)磷酸化水平下调(P<0.05)。结论碘促VEC增殖可能与胞外信号调节激酶(ERK)通路的激活有关。
Objective To investigate the relationship between iodine ion and the expression of both MEK1 and its phosphorylation during the course of vascular endothelial cell(VEC) proliferation, and to explore the pathway of the promoting effect of iodine ion on VEC proliferation. Methods 1 The vascular endothelial cells cultured in vitro were divided into the control group(without any treatment) and four KI groups(treated with 100 μg/L KI, 300 μg/L KI, 500 μg/L K and 1 000 μg/L KI, respectively). 2 The effects of iodine ion concentration(100 μg/L, 300 μg/L, 500 μg/L and 1 000 μg/L, respectively) on the expression of MEK1 and its phosphorylation were determined using Western Blot method. Results 1 The expression of MEK1 in 300 μg/L KI group was higher than that in other groups(P 0.05). 2 The MEK1 phosphorylation levels at Ser298 site in iodine ion concentration of 500 μg/L and 1 000 μg/L groups were significantly increased(P 0.05). 3 The MEK1 phosphorylation levels at Thr286 site in all different iodine ion concentration groups were significantly decreased(P 0.05). Conclusion The promotion effect of iodine ion on vascular endothelial cell proliferation is related to the activation of extracellular signal-regulated kinase(ERK) signal transduction.
出处
《介入放射学杂志》
CSCD
北大核心
2015年第2期150-153,共4页
Journal of Interventional Radiology
基金
江苏省科技创新与成果转化专项基金资助项目(BL2012021)
关键词
布加综合征
血管内皮细胞
碘离子
Budd-Chiari syndrome
vascular endothelial cell
iodine ion